Clarithromycin as an Adjunct to One-Stage Full-Mouth Ultrasonic Periodontal Debridement in Generalized Aggressive Periodontitis: A Randomized Controlled Clinical Trial.

BACKGROUND: The aim of the present study is to evaluate the periodontal clinical and microbiologic responses and possible adverse effects of clarithromycin (CLM) combined with periodontal mechanical therapy in the treatment of patients with generalized aggressive periodontitis. METHODS: Forty patients were selected and randomly assigned into one of two groups: 1) CLM (n = 20): one-stage full-mouth ultrasonic debridement (FMUD) associated with CLM (500 mg, every 12 hours for 3 days); and 2) placebo (n = 20): FMUD associated with placebo pills. Clinical and microbiologic parameters were evaluated at baseline and 3 and 6 months postoperatively. RESULTS: Both treatments presented statistically significant clinical and microbiologic improvements. However, the CLM group presented lower means of probing depth for pockets ≥7 mm at 6 months (4.0 ± 1.7 mm) compared with the placebo group (4.7 ± 1.3 mm) (P = 0.04). In addition, the CLM group also presented greater reduction of Porphyromonas gingivalis (Pg) DNA counts at 6 months (P = 0.0001). CONCLUSION: Results from this study suggest both treatments are effective; however, adjunct use of CLM to FMUD leads to better reduction of deep pockets and Pg at 6 months compared with FMUD alone.

Local levels of biomarkers after surgical and nonsurgical debridement of residual pockets and nonresidual sites in diabetic patients: a 12-month follow-up.

There is scarce evidence on suitable approaches for the treatment of unresponsive or residual periodontal sites in diabetic patients. This study assessed the effects of surgical debridement (SD) and nonsurgical debridement (NSD), associated with amoxicillin and metronidazole, on clinical and immunological outcomes of residual pockets and adjacent healthy sites in patients with type 2 diabetes. A split-mouth, randomized controlled trial was conducted in 21 patients presenting at least 2 residual pockets in contralateral quadrants 12 months after basic nonsurgical periodontal therapy. Patients received systemic antibiotics, and contralateral quadrants were assigned to receive SD or NSD. The changes in clinical parameters were evaluated from baseline to 12 months. Local levels of 14 cytokines and chemokines were measured with multiplex bead immunoassays at baseline and 3 and 12 months after therapy. There were no statistically significant differences between SD and NSD for changes in clinical parameters from baseline to 12 months (P > 0.05). There was a significantly greater increase in the levels of granulocyte-macrophage colony-stimulating factor and interleukin 6 from baseline to 3 months in the healthy sites adjacent to residual pockets receiving SD (P < 0.05). A significant decrease in the levels of monocyte chemoattractant protein-1 and macrophage inflammatory protein 1α occurred from baseline to 12 months in the residual pockets treated by SD (P < 0.05). In conclusion, SD and NSD resulted in similar clinical benefits at 12 months. The short-term increase in the levels of proinflammatory biomarkers in SD sites probably can be attributed to tissue trauma and healing, and the long-term decrease in the levels of chemotactic factors in residual pockets treated by surgery may reflect remission of infection and stable wound healing in these sites at 12 months.